Cases of Note

Cases of Note features peer-reviewed case reports and case series that document clinically relevant findings from critical and high acuity care environments. Cases that illuminate a clinical diagnosis or a management issue in the treatment of critically and acutely ill patients and include discussion of the patient’s experience with the illness or intervention are encouraged. Proposals for future Cases of Note articles may be e-mailed to [email protected].

A CASE OF THYROTOXIC PERIODIC PARALYSIS WITH RESPIRATORY FAILURE IN AN AFRICAN AMERICAN WOMAN By Denise L. Shields, MSN, ACNP-BC, CRNP

Abstract Thyrotoxic periodic paralysis is an acute endocrine emergency characterized by hyperthyroidism, profound muscle weakness and/or paralysis, and hypokalemia that is not due to potassium deficiency. Typically described in young males of Asian descent, it is becoming increasingly recognized outside of this demographic group and is believed to be an underrecognized cause of symptomatic hypokalemia. Thyrotoxic periodic paralysis usually manifests as acute onset of symmetrical distal extremity weakness and is treated with careful potassium replacement and nonselective -blockers. In this case, a 43-year-old African American woman with thyrotoxic periodic paralysis had recurrent lower extremity myopathy and acute respiratory failure precipitated by noncompliance with treatment for Graves disease. (American Journal of Critical Care. 2015;24: 264-267)

T

hyrotoxic periodic paralysis (TPP) is an acute endocrine emergency characterized by hyperthyroidism, profound muscle weakness and/or paralysis, and hypokalemia that is not due to potassium deficiency. Typically described in young males of Asian descent,1-3 it is becoming increasingly recognized outside of this demographic and is believed to be an underrecognized cause of symptomatic hypokalemia with its ensuing sequelae. Here we describe the case of a ©2015 American Association of Critical-Care Nurses doi: http://dx.doi.org/10.4037/ajcc2015910

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43-year-old African American woman with TPP who had recurrent lower extremity myopathy and acute respiratory failure precipitated by noncompliance with treatment for Graves disease.

Case Report A 43-year-old African American woman came to a community hospital for complaints of recurrent bilateral lower extremity weakness and dyspnea. The patient reported being admitted twice in the past 2 months to a tertiary facility for similar complaints where she had Graves disease diagnosed and was discharged with propylthiouracil and propranolol. Review of systems was otherwise

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negative. She denied any other past medical history but admitted to being noncompliant with the prescribed medication regimen for her Graves disease. The patient was obese with a body mass index (calculated as weight in kilograms divided by height in meters squared) of approximately 35. Radiography and computed tomography of the chest were negative for pulmonary embolism or other acute pulmonary processes. Laboratory tests revealed a thyrotropin level less than 0.005 mIU/L, free thyroxine level of 8.0 ng/dL, a potassium level of 2.8 mEq/L, and a phosphorus level of 2.4 mg/dL; remaining levels were normal and the complete blood cell count was unremarkable. Uncontrolled hyperthyroidism with hypokalemia was diagnosed, and treatment with potassium supplementation, propranolol, and methimazole was started and she was transferred to the general care area. Upon arrival in the step-down unit, the patient became nauseous with persistent complaints of lower extremity weakness and dyspnea. Neurological examination was notable for bilateral lower extremity weakness. Lungs were clear to auscultation. Telemetry showed sinus tachycardia with short bursts of nonsustained ventricular tachycardia. Her blood pressure was within normal range, pulse oximetry showed 97% saturation on 2 L oxygen, and she was afebrile. Results of arterial blood gas analysis were unremarkable. Albuterol/ipratropium nebulization was administered without improvement in her respiratory complaints. Approximately 1 hour later, the patient went into acute respiratory arrest and was intubated. Repeat testing showed a potassium level of 3.0 mEq/L; further potassium supplementation was administered. After 48 hours, the patient’s thyrotoxic state came under control with propranolol and methimazole, potassium levels normalized, and she was successfully weaned off of mechanical ventilation. She was ultimately discharged with propranolol and methimazole with instructions to follow up with an endocrinologist for possible surgical ablation of the thyroid gland as an outpatient.

Discussion Demographic Features TPP is an acute endocrine emergency that can result in severe neuromuscular dysfunction, includ-

About the Authors Denise L. Shields is an acute care nurse practitioner at Robert Wood Johnson University Hospital, Hamilton Township, New Jersey. Corresponding author: Denise L. Shields, Robert Wood Johnson University Hospital, 1 Hamilton Health Place, Hamilton Township, NJ 08690 (e-mail: DeniseShields@ verizon.net).

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ing respiratory arrest. An inherited disorder of unclear genetic cause, TPP is well documented in the Asian male population, including Japanese, Chinese, Thai, Filipino, Vietnamese, Korean, and Malaysian men.1-3 However, the growing mobility of people, immigration, and intermarriage of ethnic groups most likely account in part for the increasing prevalence of TPP in Western medicine and persons outside of this typical clinical profile. An increasing number of cases of TPP occurring across multiple ethnicities have been reported, including cases in Hispanic, African American, and white populations2 as well as a case reported involving a Turkish male.4 Lesser known is the actual incidence in females despite women having an overall higher incidence of hyperthyroid disease. Pathophysiology Although hypokalemic periodic paralysis can be a familial variant that is more common in white males and has a similar clinical presentation to the nonfamilial variant,2,3 there is no thyroid involvement and genetic mutations are well documented.3 In contrast, nonfamilial hypokalemic TPP will always have hyperthyroid abnormalities and is more prevalent in nonwhite populations. Genetic mutations have yet to be clearly identified in TPP, although some evidence indicates that it is a channelopathy defect in skeletal muscle that is partially regulated by thyroid hormones and may thus explain the correlation with an acute thyrotoxic state.5 This defect involves activity of the sodium-potassium adenosine triphosphatase (ATPase) pump that causes an acute intracellular influx of potassium ions with a subsequent decrease in extracellular potassium levels.3,4

With growing mobility and intermarriage, the prevalence of thyrotoxic periodic paralysis in Western medicine is increasing.

Provocative Factors Although a hyperthyroid state is the driving cause of the hypokalemia seen in TPP, a number of other known triggers increase susceptibility. For example, androgens are a recognized stimulant of ATPase activity, which is believed to explain the prevalence of TPP in young adult males.3,4,6 For this same reason, TPP is uncommon in women, as estrogens have the opposite effect on ATPase activity.6 Although Graves disease is the most common hyperthyroid state to evoke TPP, any cause of thyrotoxicosis, including thyrotoxic medications and thyroid nodules, can be responsible because of thyroidmediated ATPase activity. Such medications also include herbal and dietary supplements containing

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Table Clinical profiles of thyrotoxic states Thyrotoxic myopathy

Thyrotoxic periodic paralysis

Female sex Age in 40s Persistent sign and symptoms: muscle weakness and fatigue

Male sex Age in 20s Neuromuscular weakness and decreased deep tendon reflexes Signs and symptoms resolve between attacks

thyroxine, as cases of TPP due to thyroxine-based weight loss supplements have been reported.7 Additional TPP triggers include insulin2,4 and high carbohydrate intake,2,3 both of which drive potassium ions into cells and reduce serum levels of potassium. Researchers in several studies8,9 have noted TPP incidence to be higher in obese persons and persons with insulin resistance. Obesity as a provocative factor may have contributed in the case presented here; however, obesity is also associated with increased estrogen levels that would seemingly negate this effect. Steroid use has also been implicated in the occurrence of TPP,6,10-12 most likely owing to mineralocorticoids promoting excretion of potassium and corticosteroids elevating serum levels of glucose with a parallel insulin response. Additionally, any number of stressors (injury, infection, emotional turmoil) as well as exercise activate an adrenergic response that is also known to cause hypokalemic TPP in susceptible persons.2,3 The albuterol nebulizer, a known -agonist used in our female patient in attempts to alleviate her dyspnea, may have been an additional provocative factor and may even have been the final trigger of her TPP-induced respiratory failure. Clinical Manifestations Clinical manifestations include complaints of painless weakness, usually symmetrical and involving the distal parts of the extremities, but may involve proximal muscle groups and rarely the respiratory musculature (see Table). Although a thyrotoxic state is responsible for inducing hypokalemia in TPP, clinical indicators of hyperthyroidism are often absent or very subtle.2,3 Respiratory arrest due to TPP has been reported very infrequently10,13; however, respiratory arrest was an unfortunate consequence in our case study. Importantly, extreme hypokalemia is not necessary to evoke a TPP episode and has been documented to occur with mild subtherapeutic or even normal potassium levels in susceptible persons.3

Steroids, stressors, and exercise can cause hypokalemia in thyrotoxic periodic paralysis in susceptible persons.

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Even so, it does appear that the degree of myopathy matches the severity of hypokalemia.6 Hypophosphatemia is also often present3,14 and appears to play a complementary role in respiratory muscle fatigue,3 leading to respiratory failure. Electrocardiographic abnormalities consistent with hypokalemia are common in addition to tachycardia due to a hyperthyroid state. Ventricular fibrillation is a rare occurrence although it has been documented.6 Treatment and Goals of Care Goals of treatment are to prevent recurrent attacks, achieve a euthyroid state, correct hypokalemia, and minimize provoking factors.3 Initial treatment for TPP is nonselective beta-blockade (propranolol) and potassium replacement.2-4,6 Beta-blockade serves to inhibit adrenergic activity (reducing sodiumpotassium ATPase pump activity) as well as aid in the control of the thyrotoxic state. Careful supplementation with potassium is the rule. It is important to remember that aggressive replacement of potassium has been associated with rebound hyperkalemia once the myopathy begins to correct itself and is therefore avoided.2-4,6 Moreover, aggressive replacement is discouraged because TPP hypokalemia is merely reflective of intracellular potassium shifts due to a thyrotoxic state and is not a result of inherent depletion of potassium stores. Complete resolution and prevention requires strict control or abolition of the hyperthyroidism that drives this physiological response as well as the avoidance of provoking factors.3 FINANCIAL DISCLOSURES None reported. eLetters Now that you’ve read the article, create or contribute to an online discussion on this topic. Visit www.ajcconline.org and click “Respond to This Article” in either the full-text or PDF view of the article.

REFERENCES 1. Kelley DE, Gharib H, Kennedy FP, Duda RJ, McManis PG. Thyrotoxic periodic paralysis: report of 10 cases and review of electromyographic findings. Arch Intern Med. 1989;149:2597-2600. 2. Lam L, Nair RJ, Tingle L. Thyrotoxic periodic paralysis. Proc (Bayl Univ Med Cent). 2006;19(2):126-129. 3. Lin SH. Thyrotoxic periodic paralysis. Mayo Clin Proc. 2006;80(1):99-105. 4. Akar S, Comlekci A, Birlik M, et al. Thyrotoxic periodic paralysis in a Turkish male: the recurrence of the attack after radioiodine treatment. Endocr J. 2005;52:149-151. 5. Ryan DP, da Silva MR, Soong TW, et al. Mutations in potassium channel Kir2.6 cause susceptibility to thyrotoxic hypokalemic periodic paralysis. Cell. 2010;140(1):88-98. 6. Miyashita Y, Monden T, Yamamoto K, et al. Ventricular fibrillation due to severe hypokalemia induced by steroid treatment in a patient with thyrotoxic periodic paralysis. Arch Intern Med. 2006;45(1):11-13. 7. Akinyemi E, Bercovici S, Niranjan S, Paul N, Hemavathy B. Thyrotoxic hypokalemic periodic paralysis due to dietary weight-loss supplement. Am J Ther. 2011;18(3):e81-e83. 8. Soonthornpun S, Setasuban W, Thamprasit A. Insulin resistance in subjects with a history of thyrotoxic periodic paralysis (TPP). Clin Endocrinol (Oxf). 2009;70(5):794. 9. Chan A, Shinde R, Chow CC, Cockram CS, Swaminathan R.

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10.

11.

12.

13.

14.

Hyperinsulinaemia and Na+, K(+)-ATPase activity in thyrotoxic periodic paralysis. Clin Endocrinol (Oxf). 1994;41(2):213. Liu YC, Tsai WS, Chau T, Lin S. Acute hypercapnic respiratory failure due to thyrotoxic periodic paralysis. Am J Med Sci. 2004;327(5):264-267. Wongraoprasert S, Buranasupkajorn P, Sridama V, Snabboon T. Thyrotoxic periodic paralysis induced by pulse methylprednisone. Intern Med. 2007;17:431-433. Liu Z, Braverman LE, Malabanan A. Thyrotoxic periodic paralysis in a Hispanic man after the administration of prednisone. Endocr Pract. 2006;12(4):427-431. Abbasi B, Zain S, Sprabery LR. Hypokalemic thyrotoxic periodic paralysis with thyrotoxic psychosis and hypercapneic respiratory failure. Am J Med Sci. 2010;340(2):147-153. Manoukian MA, Foote JA, Crapo LM. Clinical and metabolic features of thyrotoxic periodic paralysis in 24 episodes. Arch Intern Med. 1999;159:601-606.

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A Case of Thyrotoxic Periodic Paralysis With Respiratory Failure in an African American Woman Denise L. Shields Am J Crit Care 2015;24:264-267 doi: 10.4037/ajcc2015910 © 2015 American Association of Critical-Care Nurses Published online http://www.ajcconline.org Personal use only. For copyright permission information: http://ajcc.aacnjournals.org/cgi/external_ref?link_type=PERMISSIONDIRECT

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AJCC, the American Journal of Critical Care, is the official peer-reviewed research journal of the American Association of Critical-Care Nurses (AACN), published bimonthly by The InnoVision Group, 101 Columbia, Aliso Viejo, CA 92656. Telephone: (800) 899-1712, (949) 362-2050, ext. 532. Fax: (949) 362-2049. Copyright © 2015 by AACN. All rights reserved.

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A case of thyrotoxic periodic paralysis with respiratory failure in an African American woman.

Thyrotoxic periodic paralysis is an acute endocrine emergency characterized by hyperthyroidism, profound muscle weakness and/or paralysis, and hypokal...
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